What Is Acute Renal Failure?

Acute renal failure (ARF) refers to sudden deterioration in renal function. ARF can result from multiple anatomic problems, including acute or subacute obstruction of arteries, veins, ureters, bladder, or urethra. An alternative pathophysiologic approach categorizes ARF as caused by decreased renal perfusion, ischemic or toxic cell injury, or intrinsic renal disease. When a child has ARF with oliguria, causes can be broadly categorized:

Table 65-1 has examples of oliguric ARF in each category. Remember that not all ARF is associated with oliguria.

Table 65-1 Causes of Acute Renal Failure

How Can I Tell If a Patient Has Acute Renal Failure?

Renal function is decreased in ARF. Glomerular filtration rate (GFR) is the standard measure of renal function and should be 100 ± 20 ml/min/1.73 m² body surface area (BSA) for children older than 1 year. The most accurate measure of GFR is the clearance of inulin or iothalamate, but this technique is time-consuming, invasive, and not readily available. Serum creatinine concentration is often used as a clinical marker of renal function, but it is too insensitive to identify the early stages of renal function deterioration. The commonly used assay has a wide coefficient of variation for the values found in infants and toddlers. Also, serum creatinine concentration changes during growth from infancy through adolescence as muscle mass increases and is affected to some extent by dietary protein intake.

Can Renal Function Be Estimated Easily?

The most reliable, straightforward, and simple method to estimate renal function in children uses height and serum creatinine to calculate creatinine clearance with the formula in Table 65-2. Height serves as a surrogate of muscle mass. This approach should only be used when the patient is in a steady state with respect to renal function.

Table 65-2 Formula for Estimation of Glomerular Filtration Rate (GFR) in Children*

* GFR (ml/min/1.73 m²) = [k × length or height (in cm)] ÷ serum creatinine (mg/dl). From Schwartz GJ, Brion LP, Spitzer A: The use of plasma creatinine concentration for estimating glomerular filtration rate in infants, children, and adolescents, Pediatr Clin North Am 34:571, 1987.

How Might a Patient with Acute Renal Failure Present?

ARF commonly presents with oliguria, edema, hypertension, and fatigue or lethargy. Absence of hypertension may indicate low circulating volume, as in dehydration. ARF can occur with either normal or elevated urine output, the latter especially with tubulointerstitial disease. A patient with ARF might have only vague symptoms, so it is important to consider renal causes in the differential diagnosis of the symptom complex, to look for hypertension and edema, and to consider blood and urine tests. Lethargy and altered mental status can result from accumulation of “uremic” toxins. ARF can occasionally occur in a completely asymptomatic patient. Table 65-3 lists causes, presenting features, and evaluation of ARF.

Table 65-3 Evaluation for Causes of Acute Renal Failure (ARF)

What Is Oliguria?

Oliguria means that urine output is below age-expected limits. For premature infants, oliguria is defined as urine output less than 2 ml/kg/hr. Full-term infants from birth up to 2 to 3 months of age are oliguric when urine output is less than 1 ml/kg/hr. For all others, oliguria is present when urine output is less than 0.5 ml/kg/hr.

What Is Anuria?

Anuria is the absence of urine output. It indicates either that the kidneys are not producing urine or that urine flow is completely obstructed. To determine the cause of anuria, insert a urinary catheter to determine whether the bladder is empty and obtain a renal ultrasound to look for dilatation of the collecting system and ureters.

How Can I Determine the Cause of Acute Renal Failure?

History, physical examination, and the initial laboratory tests used to diagnose the cause of ARF are listed in Table 65-3. The fractional excretion of sodium (Fe_Na) is particularly useful to differentiate acute tubular necrosis from prerenal causes, especially when urine output is low. This distinction is important because prompt intervention may facilitate renal recovery when ARF results from a potentially reversible cause, such as volume depletion. Even patients with intrinsic or postrenal causes for decreased GFR will benefit from appropriate fluid and electrolyte therapy if volume-depleted.

When Is a Renal Biopsy Indicated?

A renal biopsy is not routinely performed in ARF. Some indications for a biopsy include rapidly progressive renal failure of unexplained etiology and certain suspected causes of glomerulonephritis (see “Glomerulonephritis”).

What Are the Risks of Acute Renal Failure?

The complications of ARF arise from severe impairment of fluid excretion (hypertension and pulmonary edema) and solute clearance (hyperkalemia, hyperphosphatemia, metabolic acidosis, “uremia” causing altered mental status, and accumulation of medication metabolites).

How Do I Care for a Patient with Acute Renal Failure?

Management depends on the underlying cause. General measures include the following:

What Is Chronic Kidney Disease?

Chronic kidney disease (CKD) refers to impaired renal function, irrespective of the GFR, that persists for at least 3 months. The terms chronic renal insufficiency (CRI) and chronic renal failure (CRF) refer to the degree of GFR impairment and are no longer used. There are 5 stages of CKD based on the severity of renal impairment (Table 65-4). A patient does not need to have reduced GFR to be categorized as having CKD. A patient with stage I CKD has normal GFR with reduced renal mass, either acquired or congenital, and must be monitored for possible worsening of renal function. A patient with stage V CKD has end-stage renal disease (ESRD) and may need dialysis or renal transplantation. Loss of renal function causes impairment of other organ systems. Incidence of CKD and ESRD in children is less than 15 cases per million population in North America.

Table 65-4 Classification of Chronic Kidney Disease (CKD)

What Causes Chronic Kidney Disease in Children?

Almost 50% of all children with advanced CKD/ESRD have congenital anomalies such as hypo-dysplastic kidneys or obstructive uropathies. Other causes of CKD include renal scarring/reflux nephropathy (see “Urinary Tract Infection”) and chronic glomerulonephritis (see “Glomerulonephritis”).

How Might a Child with Chronic Kidney Disease Present?

Congenital renal anomalies are often detected on routine prenatal ultrasound. Children with obstructive uropathies may have recurrent urinary tract infections. Failure to thrive occurs commonly in infants with CKD. Children with chronic glomerulonephritis may present with gross hematuria. A relatively asymptomatic child with CKD occasionally may be identified when short stature, urinary incontinence, hypertension, or proteinuria and hematuria are discovered. Sometimes CKD is diagnosed only when a child develops complications such as uremic encephalopathy, hypertensive crisis, or pulmonary edema.

What Is the Laboratory Evaluation for Suspected Chronic Kidney Disease?

The initial laboratory approach to CKD mirrors that for ARF (Table 65-3). Laboratory tests useful in the long-term management of children with CKD include serum electrolytes, blood urea nitrogen, serum creatinine, calcium and phosphorus, parathyroid hormone level, and the complete blood count (CBC). Other tests depend on the disease that caused the CKD.

How Can I Tell If Renal Failure Is Acute or Chronic?

Clues that a patient with renal failure has CKD include the following:

Does a Renal Biopsy Help with Diagnosis?

Renal biopsy is not often needed because history, physical examination, and laboratory tests usually lead to the diagnosis. When biopsy is done, findings suggestive of CKD include severe glomerulosclerosis, interstitial fibrosis, and tubular atrophy, especially if all 3 are present. Some patients with advanced CKD undergo renal biopsy to establish the etiology, if possible, because some acquired renal diseases recur in transplanted kidneys.

How Do I Care for a Patient with Chronic Kidney Disease?

The care of a child with CKD is best performed at a tertiary care medical center with a multidisciplinary team that includes a pediatric nephrologist, a social worker, and a dietician. Management goals include efforts to do the following:

Prevent or slow the decline in renal function, if possible

Treat complications of renal failure, such as

Anemia, by using iron and erythropoietin therapy

Hyperparathyroidism, by limiting dietary phosphorus intake, using dietary phosphate binders, and prescribing vitamin D

Prevent further insults to the kidneys by avoiding nephrotoxic medications and aggressively treating hypertension and proteinuria, if present

Provide psychosocial and emotional support to the child and family

Optimize nutrition

Prepare the child for transplant or dialysis, if needed

What Is Acute Glomerulonephritis?

Glomerulonephritis (GN) is a syndrome of impaired renal function (elevated serum creatinine), some degree of oliguria, volume overload (edema, hypertension, and pulmonary vascular congestion), and hematuria of glomerular origin (see Chapter 52). It is caused by glomerular inflammation. In mild cases, hematuria may be the only sign of GN. When the onset is abrupt, GN is referred to as acute GN.

What Causes Acute Glomerulonephritis?

Causes of acute GN are listed in Table 65-5. Postinfectious GN is the most common form in children and occurs after infection by Streptococcus pyogenes (pharyngitis, or less commonly impetigo). Signs and symptoms of GN usually appear 10 to 14 days after the infection. The infection can sometimes be entirely asymptomatic. Postinfectious GN is mediated by an incompletely understood autoimmune process. In contrast, GN caused by IgA nephropathy (“Berger’s disease”) is exacerbated by infections, and symptoms appear at the same time as the intercurrent illness.

Table 65-5 Causes of Glomerulonephritis (GN) in Children

Will Acute Glomerulonephritis Cause Long-Term Complications?

Postinfectious GN is almost always self-limited, and progression to CKD is rare. Patients with acute GN caused by other disorders may develop progressive renal damage and CKD. Although self-limited, acute postinfectious GN may have life-threatening complications related to ARF, including hyperkalemia, severe hypertension, encephalopathy, seizures, pulmonary edema, and congestive heart failure.

How Do I Evaluate for Glomerulonephritis

The workup of a child with suspected GN should first establish the diagnosis, then evaluate for complications:

History: Tea- or cola-colored urine, oliguria, and edema

Physical examination: Hypertension, peripheral edema, pulmonary vascular congestion or pulmonary edema, and heart failure

Laboratory tests:

Urinalysis for blood and protein

Microscopic urinalysis for red blood cell casts

Serum creatinine (often elevated)

Serum electrolytes (hyperkalemia, acidosis)

Serum total protein and albumin (see “Nephrotic Syndrome”)

Complete blood count (dilutional anemia; thrombocytopenia in autoimmune diseases)

Chest x-ray if you suspect pulmonary edema

What Further Tests Are Needed?

The cause of GN is identified from history, physical examination, and selected tests (Table 65-6). C3 complement and anti-neutrophil cytoplasmic antibody (ANCA) levels help differentiate amongst the various causes of GN. Renal biopsy, when indicated, can identify the underlying etiology, provide information about the severity of the GN, verify a clinical diagnosis, or determine the degree of chronicity. In some diseases, such as systemic lupus erythematosus, a biopsy can distinguish the subclasses of GN, which has therapeutic and prognostic importance.

Table 65-6 Etiologic Evaluation of a Child with Glomerulonephritis